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Regulation of the BZLF1 promoter of Epstein-Barr virus by second messengers in anti-immunoglobulin-treated B cells.
Virology. 1994 Feb; 198(2):446-54.V

Abstract

Initiation of the Epstein-Barr virus (EBV) lytic cycle is dependent on the transcription of the BZLF1 gene. The BZLF1 gene promoter (Zp) was activated by crosslinking of cell surface immunoglobulin (Ig) with anti-Ig antibody in B cells, even in the absence of other viral genes. We identified several anti-Ig response elements within Zp, which were originally defined as 12-O-tetradecanoylphorbol-13-acetate (TPA) response elements (ZI repeats and ZII, an AP-1-like domain). Since anti-Ig crosslinking leads to activation of protein kinase C (PKC) and an increase in intracellular calcium level, Zp was tested for the response to these cellular factors. Treatment with calcium ionophore A23187 increased Zp activity. When the calcium ionophore was used in conjunction with TPA, a PKC activator, the Zp induction was synergistically enhanced. 1-(5-Isoquinolinyl sulfonyl)-2-methylpiperazine, an inhibitor of PKC, inhibited the anti-Ig inducibility of Zp. Calmodulin antagonists, compound R24571 and trifluoperazine, blocked the Zp activation with anti-Ig. These findings suggest that Zp responds directly to changes in the activity of both PKC and calcium/calmodulin-dependent protein kinase. Requirement of tyrosine kinase activation for the anti-Ig-mediated Zp activation was also demonstrated through the use of the tyrosine kinase inhibitor herbimycin. These cellular gene regulatory molecules induced with anti-Ig may cooperatively play an important part in achieving efficient EBV activation as seen with anti-Ig treatment in B cells.

Authors+Show Affiliations

Department of Pharmacology, University of Massachusetts Medical School, Worcester 01655.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

8291228

Citation

Daibata, M, et al. "Regulation of the BZLF1 Promoter of Epstein-Barr Virus By Second Messengers in Anti-immunoglobulin-treated B Cells." Virology, vol. 198, no. 2, 1994, pp. 446-54.
Daibata M, Speck SH, Mulder C, et al. Regulation of the BZLF1 promoter of Epstein-Barr virus by second messengers in anti-immunoglobulin-treated B cells. Virology. 1994;198(2):446-54.
Daibata, M., Speck, S. H., Mulder, C., & Sairenji, T. (1994). Regulation of the BZLF1 promoter of Epstein-Barr virus by second messengers in anti-immunoglobulin-treated B cells. Virology, 198(2), 446-54.
Daibata M, et al. Regulation of the BZLF1 Promoter of Epstein-Barr Virus By Second Messengers in Anti-immunoglobulin-treated B Cells. Virology. 1994;198(2):446-54. PubMed PMID: 8291228.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of the BZLF1 promoter of Epstein-Barr virus by second messengers in anti-immunoglobulin-treated B cells. AU - Daibata,M, AU - Speck,S H, AU - Mulder,C, AU - Sairenji,T, PY - 1994/2/1/pubmed PY - 1994/2/1/medline PY - 1994/2/1/entrez SP - 446 EP - 54 JF - Virology JO - Virology VL - 198 IS - 2 N2 - Initiation of the Epstein-Barr virus (EBV) lytic cycle is dependent on the transcription of the BZLF1 gene. The BZLF1 gene promoter (Zp) was activated by crosslinking of cell surface immunoglobulin (Ig) with anti-Ig antibody in B cells, even in the absence of other viral genes. We identified several anti-Ig response elements within Zp, which were originally defined as 12-O-tetradecanoylphorbol-13-acetate (TPA) response elements (ZI repeats and ZII, an AP-1-like domain). Since anti-Ig crosslinking leads to activation of protein kinase C (PKC) and an increase in intracellular calcium level, Zp was tested for the response to these cellular factors. Treatment with calcium ionophore A23187 increased Zp activity. When the calcium ionophore was used in conjunction with TPA, a PKC activator, the Zp induction was synergistically enhanced. 1-(5-Isoquinolinyl sulfonyl)-2-methylpiperazine, an inhibitor of PKC, inhibited the anti-Ig inducibility of Zp. Calmodulin antagonists, compound R24571 and trifluoperazine, blocked the Zp activation with anti-Ig. These findings suggest that Zp responds directly to changes in the activity of both PKC and calcium/calmodulin-dependent protein kinase. Requirement of tyrosine kinase activation for the anti-Ig-mediated Zp activation was also demonstrated through the use of the tyrosine kinase inhibitor herbimycin. These cellular gene regulatory molecules induced with anti-Ig may cooperatively play an important part in achieving efficient EBV activation as seen with anti-Ig treatment in B cells. SN - 0042-6822 UR - https://www.unboundmedicine.com/medline/citation/8291228/Regulation_of_the_BZLF1_promoter_of_Epstein_Barr_virus_by_second_messengers_in_anti_immunoglobulin_treated_B_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0042-6822(84)71056-7 DB - PRIME DP - Unbound Medicine ER -